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One man’s junk is another man’s critical regulator of the first stages of embryonic development.

The so-called “jumping gene,” long considered hereditary clutter or a damaging parasite, is actually key to human evolution.

Transposable elements (TEs), or transposons, are DNA sequences that duplicate and reinsert themselves into different locations on the genome (hence “jumping”).

First identified 50 years ago by geneticist Barbara McClintock, transposons are found in almost all organisms, typically in large numbers (they make up 50 percent of the human genome).

But while many stowaways are harmless, others wreak havoc by altering or disrupting cells’ normal programming, according to the University of California San Francisco. TEs have been associated with diseases like cancer.

New research, however, suggests that the most common transposon, LINE1, is actually necessary for embryos to develop past the two-cell stage.

Analyzing TEs since 2003, senior author Miguel Ramalho-Santos, an associate professor of obstetrics/gynecology and reproductive sciences at UCSF, recalls his early days studying LINE1.

“Given the standard view of transposons, these early embryos were really playing with fire,” he said in a statement. “It just didn’t make any sense, and I wondered if something else was going on.”

The project took off when Michelle Percharde joined Ramalho-Santos’s lab as a postdoc researcher in 2013.

“When I saw all the LINE1 RNA that’s present in the nucleus of developing cells, I agreed there must be some role it’s playing,” she said.

Using mouse embryos, the pair performed experiments to eliminate LINE1 RNA from rodent embryonic stem cells, and the results were surprising: The pattern of gene expression in the cells completely transformed.

“When we saw that cells were changing identity when we moved LINE1 RNA, that was our real ‘Aha!’ moment that told us we were on to something,” Percharde said.

After five years—and various new techniques for studying transposons—researchers hope their findings can convince others to stop villainizing jumping genes.

“These genes have been with us for billions of years and have been the majority of our genomes for hundreds of millions of years,” Ramalho-Santos said. “I think it’s fair to ask if the 1.5 percent of protein-coding genes are the free-riders, and not the other way around.

“We now think these early embryos are playing with fire, but in a very calculated way,” he added.

Ramalho-Santos and Percharde’s full findings were published this week in the journal Cell.